Drugs that I always see and never know... Flashcards
Cyclophosphamide: MOA, use
- alkylating agent that cross-links DNA ==> apoptosis
- uses
- non-Hodgkin’s lymphoma
- breast/ovarian cancer
Naloxone
MOA: mu-opiod receceptor antagonist
use: opiod/heroin overdose
Flumazenil
- MOA:
- use: benzodiazepine antagonist/overdose
Haloperidol
- MOA:
- Use
- anti-psychotic
- delirium
- tranquilization in agitated patient
Lorazepam
- Benzodiazepine
- MOA: allosteric modification of a specific kind of neurotransmitter receptor, the GABAA receptor, which increases the overall conductance of these inhibitory channels
- Use:
- acute anxiety
- status epilepticus
Morphine: MOA
- agonist @ Mu opioid receptors
- Mu opoid receptors = GPCR ==>
- activation of K channels ==> increased K efflux
- ==> hyperpolarization ==> termination of pain signaling from nerves
Isoproteronol MOA
- agonist at B1 and B2 receptors w/no alpha receptor activity ==>
- increase in cardiac contractility (B1)
- vascular smooth muscle relaxation (B2)
Tx of acute mania
- mood stabilizers = lithium, valproate, carbamazepime
- atypical antipsychotic = olanzapine
colchicine: MOA/use/SE
- inhibition of microtubular polymerization ==> prevention of aggregration ==> disrupts chemotaxis and phagocytosis
- also inhibits formation of leukotriene B4
- use = acute gouty arthritis
- SE = nausea, abdominal pain, diarrhea
Enoxaparin: MOA
- low molecular weight heparin
- MOA: binding and activating antithrombin III
- active ATIII prevents factor Xa from: prothrombin ==> thrombin
- ==> anticoagulant effect
Digoxin clearance
via kidneys
Glucorticoids stimulate…?
liver (gluconeogenesis/glycogenolysis)
Valproate during pregnancy ==> ?
- neural tube defects due to inhibition of folic acid absorption @ intestine
- meningocele, spina bifida, etc.
Ebstein’s anomaly association/presentation
- “Ebstein’s anomaly” = “atrialization” of R ventricle due to downward displacement of tricuspid valve
- associated w/mother use of lithium during early pregnancy
Tx/recommendations after total gastrectomy
- parental B12
- to avoid dumping syndrome (colicky ab pain, nausea, diarrhea)
- small meals
- low dietary intake of simple sugars
Isoniazid side effects
- peripheral neuropathy (if given w/pyroxidine)
- hepatotoxicity
- usually mild ==> transient elevated AST, ALT
- elevated bilirubin
- fever, anorexia, nauseau
- severe ==> liver dysfxn, jaundice, bilirubinuria
Hib vaccine + importance
- composed of polyribosyl-ribotol-phosphate (PRP) = component of Hib capsule
- [conjugated w/diptheria or tetanus toxoid]
- ==> lasting immunity against Hib in children
- H. flu ==> epiglottitis
Raloxifene: MOA
- SERM
- estrogen agonist @ bone ==> prevention of osteoporosis
- estrogen antagonist @ breast ==> prevention of breast cancer
Atenolol: MOA + effects
- B1 receptor antagonist
- @ cardiac tissue and JGA, but not @ vascular smooth muscle
- ==> decreased cAMP @ cardiac/renal
Tx of organophosphate poisoning
- Atropine: reversal of muscarinic sx; no effect on nicotinic receptors
- pts still at risk for muscle paralysis
- Pralidoxime: reverses muscarinic and nicotinic effects of organophosphates
- effective only if given early after the exposure
Drug effects:
tachyphylaxis =
additive =
synergistic =
permissive =
- tachy = decreased drug response w/repeated administration
- additive/synergistic = two drugs with similar actions
- additive = admin of both is equal to the sum of the effects
- synergistic = admin of both leads to effects exceeding the sum of the drugs individually
- permissive = admin of a different type of drug (without its own action @ desired site) leads to increased action of an effective drug if given together
AChE in amniotic fluid ==> dx?
- Neural tube defects = failure of fusion of neural tube during 4th week of fetal development
- ==> leakage of fetal CSF ==>
- elevated alpha-fetoprotein
- crosses placenta ==> elevated alpha-fetoprotein @ mother serum
- acetylcholinesterase
- elevated alpha-fetoprotein
Iodine transport @ thyroid
- sodium-iodide symporter brings iodine into thyroid against concentration gradient
- NIS is also responsible for transporting perchlorate and pertechnetate into thyroid
- if potassium perchlorate is present ==> competitive inhibition
Drugs that interfere with iodine uptake
- antithyroid thionamides
- methimazole ==I thyroid peroxidase ==> blocked conversion of iodide to iodine
- propylthiouracil
- usually stopped 7-10 days before tx w/radioactive iodine for hyperthyroidism
Dobutamine impact on pressure-volume loop
- ==> increased contractility
- ==> higher pressures during ventricular ejection phase + greater volume expelled
- ==> widening of P-V loop
Tx for severe asthmatics
- anti-IgE drugs to help reudce allergy triggers of asthma
- e.g. Omalizumab ==> patients w/mod-severe allergic asthma
- IgG1 monoclonal antibody
- binds to IgE to prevent action of IgE w/its receeptor on mast cells ,basophils and other cells
Anti-metabolite drugs
- Folate antagonist
- Methotrexate
- Purine Analogs
- 6-thiopurines
- 6-mercaptopurine
- 6-guanopurine (?)
- Fludarabine ==> CLL tx
- Cladribine ==> HCL tx
- 6-thiopurines
- Pyrimidine Ananologs
- 5-FU
- Capecitabine
- Cytarabine
- Gemcitabine
Vinblastine: MOA, SE
- MOA:
- inhibits MT formation of mitotic spindle
- SE:
- alopecia
- constipation
- myelosuppression
- neurotoxicity (rare)
Cancer drugs that act in the M phase of the cell cycle
- vinca alkaloids=inhibit MT fxn/spindle formation
- vincristine
- vinblastine
- paclitaxel
- binds to tubulin and hyperstabilizes MTs that have already polymerized ==> prevents spindle breakdown
5-fluorouracil: MOA, use
- anti-metabolite
- prevents formation of thymidine vua inhibition of thymidylate synthase
- uses
- slow-growing solid tumors:
- breast
- ovarian
- pancreatic
- colorectal
- gastric carcinomas
6-mercaptopurine: MOA, use
- anti-metabolite
- inhibits formation of purines
- use = cancer drug
Methotrexate: MOA, use
- anti-metabolite
- inhibts dihydrofolate reductase ==> inhibition of DNA synthesis (via same pathway as 5-fluorouracil)
- use = cancer drug
Busulfan: MOA, use
- DNA alkylating agent (cell cyle nonspecific)
- use = CML
Bleomycin: MOA, use, SE
- inhibit replication by inducing DNA strand breaks via free radical formation
- strand breakage interrupts G2 phase of cell cycle (after DNA synthesis)
- uses: testicular tumors, lymphomas, squamous cell carcinoma
- SE
- rales, cough
- infiltration ==> fibrosis
Cyclophosphamide: MOA, uses, SE
- DNA alkylating agent (cell cycle nonspecific)
- activated by CYP450
- ==> apoptosis via DNA crosslinking
- uses
- leukemias, lymphomas
- testicular and gyn cancers
- SE
- hemorrhagic cystitis
How to prevent major side effect of cycloposphamide
- prevent hemorrhagic cystitis via:
- adequate hdration
- IV injection of mesna
Methotrexate rescue
- folinic acid aka n-formyl-xxxx aka leucovorin
- acts synergystically with 5FU
Common method of chemotherapy resistance
- human multi-drug resistance gene (MDR1)
- p-glycoprotein = transmembrane ATP-dependent efflux pump
- broad specificity for hydrophobic compounds
- decreases drug entry and increases efflux
Diuretic overuse impact on blood pH/gases
- diuretic overuse ==> compensatory increase in aldosterone
- aldosterone ==> sodium + H2O retention + K+ and H+ loss @ kidneys ==> metabolic alkalosis
- “contraction alkalosis”
- labs = high pH, high HCO3, high pCO2
Characteristics of drugs w/various volume of distribution
- low Vd = 3-5 L
- highly bound
- charged
- hydrophillic
- high molecular weight
- Vd = 14-16L = plasma + interstitial fluid
- small molecular weight
- hydrophillic
- Vd = 41L = highest distribution
- lipophillic (or hdyro)
- uncharged
Isoniazid: MOA
- antimycobacterial
- inhibits mycolic acid synthesis
Buspirone: MOA/properties, use
- MOA: partial 5HTA1 agonist
- no muscle relaxant
- no anti-seizure
- little hypnosis/hallucinatory
- Use:
- anxiety
- esp. @ previous abusers of anxiolytics
- less addiction potential vs. benzos
a1 receptors location + effect + drugs (agonists)
- pupil sphincter ==> mydriasis (dilation)
- bladder ==> sphincter contraction
- peripheral blood vessels ==> increased SBP
- agonists
- norepi
- epi
- phenylephrine
- methoxamine
beta-1 receptor locations + effects + agonist drugs
- heart ==> increased HR, contractility
- agonsits
- epinephrine
- dobutamine
- dopamine
- isoproteronol
beta-2 receptor locations + effects + agonist drugs
- bronchi ==> bronchodilation
- uterus ==> relaxation
- skeletal muscle bood vessels ==> vasodilation
- agonist drugs
- isproteronal
- terbutaline
- ritodrine
How long till continuous infusion or drug reaches steady state?
- IF: continuous infusion + elimination via first-order kinetics ==>
- steady state plasma concentration @ 4-5 half lives
Presentation of ethylene glycol toxicity
- ethylene glycol metabolized ==> glycolic acid & oxalic acid
- anion-gap metabolic acidosis
- calcium oxalate crystals in urine
- increased osmolar gap
- acute kidney injury/renal failure
- damage to tubular epithelium
- vacuolization
- ballooning
- damage to tubular epithelium
Presentation of theophylline toxicity + tx
- theophylline ==>
- N/V + abdominal pain
- arrhythmias
- seizures **
- Tx
- gastric lavage
- activated charcoal
- cathartics (increase elimination via GI tract)
- beta-blockers ==x arrhythmias
- benzodiazepines & baribituates ==x seizures
Lithium: indications, side effects
- bi-polar; manic and depressive episodes, maintenance
- SE
- DI
- tremor
- hypothyroidism
- Epstein’s anomaly
Valproate: indications, SE
- manic episodes; maintence in bipolar & generalized/absence/myclonic seizures
- SE
- hepatotox
- NTDs
Carbamazepine: indications, SE
- manic episodes, maintence
- partial generalized seizures
- trigeminal neuralgia
- SE
- agranulocytosis
- NTDs
- hyponatremia (SIADH)
Lamotrigine: indications, SE
- depressive episodes, maintenance in bipolar
- focal seizures
- SE
- stevens-johnson
- benign rash
Mood stabilizers in bipolar
- lithium
- valproate
- carbamazepime
- lamotrigine
Use/Effects:
Physostigmine vs. Neostigmin vs. Edrophonium
- all AChE inhibitors
- use = reverse atropine toxicity
- neostigmine/edrophonium = only fxn @ peripherphy; cannot penetrate CNS
- physostigmine = fxns @ periphery & CNS
5HT3-inhibitors
- ondansetron
- granesetron
- dolasetron
Rapid and complete relief in RA [short-term]
glucocorticoids, e.g. prednisone
Nevirapine: MOA, similar drugs
- NNRTI
- inhibits reverse transcription, doesn’t need phosphorylation to be active
- other drugs
- efavirenz
- delaviridine
Canagiflozin: MOA, use, SE
- MOA
- oral anti-diabetic
- = SGLT2 inhibitor ==> decreased reabsorption of glucose @ proximal renal tubule
- ==> urinary glucose loss
- SE
- renal effects
Lithium toxicity antidote
hydrocholorthiazide ==> trapping in urine
thiopental: moa, use
- lipid-soluble barbituate used as short-term anesthesia
- ==> brain ==> rapid redistribution to skeletal muscle and adipose tssue (w/in 5-10min)
- rapid redistribution allows for short term anesthia
Characteristics of serotonin syndrome
- occurs when SSRIs are given in conjunction w/other serotonergic agens
- sx
- neuromuscular excitation: hyperreflexia, clonus, myoclonus, rigidity
- autonomic stimulation: hyperthermia, tachycardia, diaphoresis, tremor
- AMS
Examples of serotonergic agents
- Anti-depressants
- monoamine oxidase inhibitors
- TCA
- SNRI
- analgesics
- tramadol
- anti-emetics
- 5-HT3 receptor antagonists (ondansetron)
- antibiotics
- linezolid = weak monoamine oxidase inhibitor
- neuropsych
- triptans
Tx tp prevent recurrences of genital herpes
- daily treatment with oral valacyclovir, acyclovir, or famciclovir ==> suppression of reactivation
Amphotericin B: MOA, SE
- MOA = binds ergosterol ==> pores ==> cell death
- SE
- renal toxicity
- ==> vasoconstrict ==> decreased GFR
- direct toxin to renal epithelial cells ==> ATN, renal tubular acidosis, and electrolyte distrubances
- **hypoK and hypoMg
- ==> decreased EPO ==> normochromic, normocytic anemia
Antifungal that inhibits fungal cell wall synthesis
- Capsofungin
- inhibits synthesis of cell wall polysaccharide glucan
Phenytoin SE/toxicity
- CNS effects ==> cerebeller defects/ataxia
- gingival hyperplasia
- pheny ==> increased PDGF ==> stimulated macs to proliferate gingiva and alveolar bone
- coarsening of facial features, hirstruism
- interferes w/folic acid metabolism ==> megaloblastic anemia
- induces P450
- teratogen ==> fetal hydantoin syndrome
Phenelzine: drug class, use, other similar drugs
- MAOIs
- Atypical depression = mood reactivity (to positive events), leaden fatigue, rejection sensitivity, increased sleep and apetite
- others
- tranylcypromine
Rare, serious side effect of ACE-i
- angioedema = face, lips, tonuge, eyelids, larygneal edema ==> difficulty breathing
- most likely due to elevated bradykinin levels
SE: Orange/red body fluids ==> drug + MOA?
- Rifampin
- ihibits DNA-dependent RNA synthesis (bacterial RNA pol)
Contraindications for use of OCPs
- Prior thromboembolic event/stroke
- hx of estrogen-dependent tumro
- women > 35 who smoke heavily ==> higher risk of CV events
- hypertriglyceridemia
- decompensated or active liver disease
- pregnancy
Causes of exacerbation of mysathenia gravis
- myasthenic crisis = undertx
- cholinergic crisis = overtx
Antidote for serotonin syndrome
- cyproheptadine = antihistamine + anti-serotonergic properties
Verapamil: MOA, use, SE
- MOA = non-dihydropyriddine ca-channel blocker
- slows conduction through AV nodes
- use = rate control in afib w/rapid ventricular response
- SE
- constipation
- gingival hyperplasia
- bradycardia
- first, second, or third degree AV node block
Leoprolide impact @ male
- GnRH
- transient increase, then decrease in both T and DHT
Vancomycin: MOA vs. Ceftriaxone: MOA
- Vanc binds D-ala (glycoproteins @ cell wall of bacteria)
- Ceftriaxone binds PBPs
- PBPs = transpeptidases that cross-link peptidoglycan @ cell wall
Beta blocker effects in thyrotoxicosis
- decrease noradgrenergic responses
- decreased T4 ==> T3 conversion @ periphery
Anti-pseudomonals
- Pip-Taz
- [some] Cephs
- Cefatadazine
- Cefepime
- Gentamicin
- [some] fluoro
- ciprofloxacin
- levofloxacin
- carbapenems
Heparain: MOA
- binds antithrombin III and increases action
Drug-induced lupus: association
- drugs metabolized by liver acteylation
- hydralizine
- procainamide
- slow-acetylators are @ higher risk
Mast stablizing agents
- cromolyn
- nedocromil
- inhibit mast cell degranulation regardless of stimuli present
- 2nd line for tx of allergic rhinitis and bronchial asthma
Niacin SE
- vasodilation ==> flushing
- can potentiate anti-htn meds ==> dosage decrease
- ==> increased insulin resistance
- ==> dosage increase in DM meds
Acetozolamide: MOA, use
-MOA: inhibits CA @ proximal tubule ==> excretion of HCO3- + sodium ==> diuresis + alkaline urine + metabolic acidosis -use: open & close-angle glaucoma, others
DRESS syndrome
-Drug Rxn with Eosinophilia & Systemic Sx -2-8 weeks after starting new medication -esp. anticonvulsants, antibiotics, allopurinol, sulfonamides -fever, general lymph, facial swell, eosino, skin rash, organ dysfxn
Drug-induced lupus
-hydralazine (HTN drug, arteriolar vasodilator via K channel binding) -procainamide -isoniazid
opioid drug that can produce w/drawal in someone on morphine
pentacozine
Selegiline: MOA
MAO-B inhibitor
Methotrexate toxicity antidote
Folinic acid
Characteristics of digoxin toxicity
-nonspecific GI = N/V, abdominal pain, anorexia -neurologic = fatigue, confusion, weakness, sometimes: color vision changes -most serious complication = arrhythmias
Drugs not to use with partially occluded coronary arteries
-coronary artery vasodilators -vasodilation of unoccluded arteries ==> reduced blood flow through collaterals to ischemic areas ==> worsening ischemia
Which of these drugs would cause bradycardia: -Nifedipine -Captopril -Verapamil -Isosorbide nitrate -Prazosin
-verapamil only -all others act peripherally
Drugs with negative chronotropic effects @ heart
-B-blockers -non-dihydropyridine Ca-channel blockser (verapamil, diltiazem) -cardiac glycosides (digoxin) -Amiodarone and sotalol -Cholinergic agonists (pilocarpine, rivastigmine)
Drug effect of sildanefil is similar to what naturally occuring hormones/mechanisms
- NO 2. ANP all ==> increased cGMP
DDAVP: moa, use
-vasopressin analog -little affect @ V1 receptors ==> no vasoconstriction -use: 1. central DI 2. bleeding control: induces release of procoag proteins (e.g. vWF) and stabilized factor VIII (Hemo A)
High vs. low potency antipsychotics
high = fluphenazine, haloperidol low = chlorpromazine, thioridazine
Class of anti-arrhythmics that show “use-dependence” + example
-class I anti-arrhymics (Na-cahnnel blockers) -IC = strongest association w/Na; slow to leave ==> prolonged QRS, but no effect on overall AP ==> normal QT
Carbamazepime: MOA, use, SE
-MOA = blocks VSSC @ neurons -use = partial, partial complex, gen TC seizures + mood stabilizer -SE = bone marrow suppression
Gq receptor pathway
- binding ==> phospholipase C converts mem. phospho ==> IP3 & DAG 2. IP3 ==> increased Ca release from SR 3. Ca + DAG activate PKC 4. PKC phosphorylates 2nd mess ==> downstream effects
Ethambutol SE
optic neuritis, color blindness ,etc.
Nitrate with highest bioavailability
isosorbide mononitrate
Antidote for NE drip-mediated tissue necrosis
-alpha-1 receptor blocker -e.g. phentolamine
Tx of calcium oxalate kidney stones
hydrochlorothiazide: blocks Na/Cl transporter @ lumen ==> activation of Na/Ca exchanger ==> increased Na w/in cell in exchange for increased Ca reabsorbed
Adenosine: MOA, use, SE
-MOA: slowing conduction through AV node by hyperpolarizing nodal & conducting cells -use: drug of choice in paroxysmal SVT -SE: flushing, chest buring (bronchospasm), hypotension, high-grade AV block
Reason for methodone use
- used to help patients recover from heroin addiction
- very long half-life opioid agonist w/good oral bioavailablity
- prevents withdrawal sx while weaning off heroin
Common causes of myopathy with elevated CK
- inflammatory myopathy
- skin rash and inflammatory arthritis may also be present
- statin-induced
- hypothyroidism
- hypothyroid sx present
- myoedema = mounding of m. after percussion
Ipratropium: MOA, use
- Muscarinic antagonist @ bronchial smooth m.
- less effective than B2 agonists
- enhance B2 agonists
- use in asthma
Theophylline: MOA, use
- MOA: inhibit phosphodiesterase ==> increased cAMP ==> bronchial sm. m. dilation
- use: asthma
Nicotinic receptors
- ligand-gated ion channels
- ACh binding ==> immediate influx of Ca2+ and Na+ and efflux of K+
Clozapine: MOA, use, SE
- MOA: blocks D4 receptors
- use: refractory psychosis/schizophrenia
- SE
- agranulocytosis
- seizures
Insulin types
- Basal/long-acting
- Glargine; Determir = once daily
- NPH = twice daily
- Short-acting/post-prandial
- Regular = best for IV
- Lispro, Aspart, Glulisine = peak @ 45 min - hour
- best for post-prand hyperglycemia
Common disinfectant mechanisms:
alcohols
chlorhexadine
hydrogen peroxide
iodine
- alcohols
- disruption of cell membranes
- denaturation of proteins
- chlorhexadine
- disruption of cell membranes
- coagulation of cytoplasm
- hydrogen peroxide
- free radicals
- sporocidal
- iodine
- halogenation of proteins & nucleic acids
- sporocidal
Tx of idiopathic pulmonary HTN
Bosentan = endothelin antagonist ==> vasodilation @ pulm. artery
Sotalol: MOA, SE
- MOA
- K+ channel blocker
- mild B-blocker effects
- Class 3 anti-arrhythmic
- amiodarone
- ibutilide
- dofetilide
- SE
- mild bradychardia
- prolonged QT interval
First-line drug for benign essential tremor + SE
- Primidone ==> active metabolites = phenobarbitol (+ phenylethylmalonimide) ==> anticonvulsant effects
- must monitor levels ==> AMS, sedations
Hyperthyroid sx that does not improve w/beta blockers
exopthalmos = due to fibroblast proliferation and ground substance production
Drug that ==> vasodilation + blocks platelet agg. used in PAD
Cilosotazol
Isoniazid: MOA, resistance
- inhibits mycolic acid formation
- must be processed by mycobacterial catalse-peroxidase to become active
- resistance:
- change mycolic acid structure/isoniazid binding site
- decreased activity of catalase-peroxidase
Glucagon receptor type + other hormones w/same receptor
- G-protein coupled receptor
- binding ==> activated Adenylate Cyclase ==> increased cAMP ==> activated PKA
- other hormones
- PTH
- B-andrenergic
- TSH
Metoprolol effects
- B1 selective blocker
- present @ heart & JGA
- ==> decreased HR
- ==> blocks renin release by JGA cells
V2 effects @ medullary collecting duct
- ==> increased permeability to H20 and urea
Initial treatment of severe hypoglycemia
- in the field/@home:
- less severe (mild-moderate) ==> fast-acting carbs; e.g. fruit juice, glucose tablet
- unconscious: IM glucagon
- @ hospital: IV glucose
Tx for combined T-C and absence seizures
- valproic acid
Amphotericin B: SE
- Nephrotoxicity and electrolyte abnormalities
- ==> hypoK and hypoMG
- hypoK ==> T wave flat, ST-depression, U waves
Bethanacol: MOA
musc. antagonist
Calcinuerin fxn
- calc = protein phosphatase ==> dephosph NFAT ==> trxn factor for IL-2 ==> T cell growth and maturation
- Cyclosporine & Tacrolimus ==I calcineurin ==> anti-rejection/immunosuppress drugs
Unfractionated vs. LMWH
- unfractionated = binds ATIII and allows activity against factor Xa and thrombin (inactivation)
- LMWH ==> ATIII activity against Xa only
Insulin receptor mechanism
- insulin ==> tyrosine kinase ==> insulin receptor substrate phosphorylization ==> activation of protein phosphatase
- protein phosphatase ==> dephosph glycogen synthase = activated glycogen formation
- also ==> dephosph of fructose-1,6-bisphosphatase = inactive ==> inhibition of gluconeogenesis
Succinylcholine: MOA, use
- MOA: depolarizing NMJ blocker
- use: rapid induction/intubation or for surgical intubation
- phase I = augmented by AChEi (e.g. neostigmine)
- phase II = reversed by AChEi
Methotrexate SE
- stomatitis = painful mouth ulcers
- hepatotoxicity = hepatitis, fibrosis, cirrhosis
- myelosuppression ==> increased infection risk
- B-cell lymphomas
- pulmonary fibrosis
- contraindicated in pregnancy
Terbanifine: MOA
- inhibits squalene oxidase ==> inhibition of fungal wall formation
- use = dermatophytoses; e.g. tinea corporis
Fluoroquinolones: MOA
- bactericidal
- inhibit DNA topoisomerase activity
Fluoroquinolones: adverse effects
- GI upset
- damage to cartilage @ children
- tendinitis/tendon rupture in adults
- mild
- H/A
- dizziness
- rash
Aminoglycosides: MOA
- bactericidal
- block bacterial protein synthesis through inhibition of 30S ribosomal unit
Aminoglycosides: adverse effects
- nephrotoxicity
- ototoxicity
Macrolides: MOA
- bacteriostatic
- blocks protein syntehesis at 50S ribosomal unti
Macrolides: adverse effects
- GI discomfort
- acute cholestatic hepatitis
- eosinophilia
- skin rashes
- more severe
- pseudomembranous colitis
- ventricular arrhythmias
Tetracyclines: MOA
- bacteriostatic agents
- block protein synthesis by actin at 30S ribosomal subunit
Tetracyclines: adverse effects
- GI distress
- tooth discoloration
- inhibition of bone growth @ children
- photosensitivity rxns
- more severe
- bacterial superinfection
- hepatotoxicity
Trimethoprim-sulfamethoxazole: MOA
- trimethoprim-sulfamethoxazole
- MOA = inhibitis bacterial folate synthesis via inhibition:
- dihydropteroate synthetase (trimetho) and dihydrofolate reductase (sulfa)
Penicillins: MOA
- bactericidal
- inhibition of cell wall synthesis via inhibition of cross-linking of peptidoglycan
Cisplatin: MOA, SE
- MOA: reactive oxygen species ==> DNA crosslinks
- SE
- nephrotoxicity: acute tubular injury
- antidote/prevention = amifostine + IV normal saline (chloride diuresis)
- thiol-based cytoprotective free-radical scavenging agent
- ==> decreased nephrotox
- antidote/prevention = amifostine + IV normal saline (chloride diuresis)
- nephrotoxicity: acute tubular injury
Argatroban: MOA, use, similar drugs
- binds thrombin active site ==> direct thrombin inhibition
- ues = HIT
- other drugs
- hirudin
- lepirudin
Anastrozole: MOA, use
- MOA: aromatase inhibitor ==> inhibition of estrogen synthesis
- use: metastatic breast cancer
